AB0483 THE ROLE OF PENTRAXIN-3 AS PREDICTOR OF PREGNANCY COMPLICATIONS IN PATIENTS WITH SLE AND/OR ANTI-PHOSPHOLIPID SYNDROME
Authors: M. Larosa, A. Calligaro, M. Tonello, A. Ghirardello, T. Del Ross, M. Favaro, L. Iaccarino, A. Doria
Journal: Annals of the Rheumatic Diseases (2022)

Background Pentraxin-3 (PTX3) seems to be implicated in placentation and foetus tolerance, being mostly secreted in response to inflammatory stimuli by dendritic cells, macrophages, and endothelial cells (1). Although several studies have recently focused on this molecule (2-4), no data on women with SLE/APS are available to date. Objectives To assess the role of serum PTX3 and anti-PTX3 Abs as predictors of pregnancy complications in SLE and/or APS. Methods This case control study included pregnancies in women with SLE (SLICC, 2012) and/or APS (Miyakis, 2006), recruited at University of Padova in the Out-patient Clinic shared by Obstetrics and Gynaecologists and Rheumatologists. The control group included pregnancies of patients with other rheumatic diseases rather than APS and/or SLE. All pregnancies were recruited from 2015 to 2021 (conception date&lt; 1 st Apr 2021). At first-trimester consultation, demographics, clinical, and serological variables were recorded. First-trimester serum PTX3 levels (ng/ml) were detected by a commercially available sandwich ELISA (Alexis, UK); IgG anti-PTX3 Abs were detected by home-made validated ELISA and expressed as Optical Density values, measured at 405 nm by microplate spectrometer. Cut-off of positivity corresponded to 0.234 OD. Maternal complications included SLE flares (increase of ≥1 point in SLEPDAI); preeclampsia/eclampsia, HELLP, pregnancy induced hypertension, maternal death, gestational diabetes mellitus (GDM). Foetal complications included: miscarriage&lt;10 week of gestation (WG); intra-uterine foetal death (IUFD) (≥10 WG); preterm delivery (&lt;37 WG); intra-uterine growth restriction (IUGR); neonatal death within 28 days from birth. Results 79 pregnancies occurred in 79 patients (Table 1). Serum IgG anti-PTX3 Abs were found in 11 women (13.9%, 95% CI 7.2-23.5), and they did not differ between cases and controls (p=0.08, 4 SLE/APS women vs. 7 controls). Anti-PTX3 were associated with GDM (p=0.04, stratified for maternal age) but not with IUGR (p=0.09). No other statistical associations were found between anti-PTX3 Abs and other maternal/foetal complications. PTX3 serum levels did not statistically differ between cases and controls (p=0.63, 0.37 ± 0.26 ng/mL in cases vs. 0.33 ± 0.24 ng/mL in controls). Serum PTX3 levels were lower in patients with GDM (0.3 ± 0.2 ng/mL) compared to non-GDM patients (0.4 ± 0.2) but it did not differ between IUGR and non-IUGR, although the mean PTX3 ± SD was lower in the IUGR group (0.25 ± 0.2 in IUGR vs 0.35 ± 0.2 in non-IUGR). Table 1. Clinical and serological characteristics of our cohort (N=79 ) Patients (N, % ) Age at pregnancy, years (mean ± SD) 35.1 ± 3.9 Cases 13 (16.5) SLE 9 (11.4) APS 7 (8.9) SLE with secondary APS 3 (23.1) Control Group 66 (83.5) Serological features LAC 11 (13.9) IgG/IgM anti-cardiolipin 20 (25.3) IgG/IgM antibeta2-Glycoprotein I 25 (31.6) Triple positive aPL tests 6 (7.6) Primiparous 23 (29.5) IgG anti-PTX3 Abs 11 (13.9) IgG anti-PTX3 level (cut-off 0.234 OD), (median, IQR) 0.2 (0.1-0.2) PTX3 ng/mL (mean ± SD) 0.3 ± 0.2 Concomitant treatment Heparin 15 (19.0) Aspirin 44 (55.7) Immunosuppressants 3 (3.8) Hydroxychloroquine 21 (26.6) Prednisone 9 (11.4) Prednisone dosage (mg/day) (median, IQR) 5 (2.5-7.5) Legend to Table 1: SD: standard deviation; SLE: Systemic Lupus Erythematosus; APS: antiphospholipid syndrome; LAC: Lupus anticoagulant; aPL: antiphospholipid antibodies; PTX: Pentraxin-3; Abs: antibodies; OD: optical density; IQR: interquartile range. Conclusion To our knowledge, this is the first study which assessed the frequency of anti-PTX3 Abs in a cohort of SLE and/or APS pregnant women. These Abs occurred in the minority of patients (13.9%) and did not differ between SLE/APS women and controls. Due to our sample size, these findings need to be confirmed in larger cohorts. References [1]Cruciani L, et al. Journal of Perinatal Medicine, 2010:38. [2]Akolekar R, et al. Prenat. Diagn. 2009;29:934–8. [3]Bassi N, et al. Clinic Rev Allerg Immunol 2015;49:217–26. [4]Gatto M, et al. Journal of Autoimmunity, 2016;74:208–16. Disclosure of Interests None declared